ArticleOncotarget2017
FOXO3 induces ubiquitylation of AKT through MUL1 regulation.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Inactivation of mitochondrial MUL1 E3 ubiquitin ligase deregulates mitophagy and prevents diet-induced obesity in mice.Frontiers in molecular biosciences · 2024Article
- Review
- Myristate induces mitochondrial fragmentation and cardiomyocyte hypertrophy through mitochondrial E3 ubiquitin ligase MUL1.Frontiers in cell and developmental biology · 2023Article
- Regulation of Metabolism by Mitochondrial MUL1 E3 Ubiquitin Ligase.Frontiers in cell and developmental biology · 2022Article
- UBXN7 cofactor of CRL3Biochimica et biophysica acta. Molecular cell research · 2021Article
- The emerging roles of E3 ubiquitin ligases in ovarian cancer chemoresistance.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- Mitochondrial MUL1 E3 ubiquitin ligase regulates Hypoxia Inducible Factor (HIF-1α) and metabolic reprogramming by modulating the UBXN7 cofactor protein.Scientific reports · 2020Article
- miR-629 targets FOXO3 to promote cell apoptosis in gastric cancer.Experimental and therapeutic medicine · 2020Article
- Non-thermal plasma treated solution with potential as a novel therapeutic agent for nasal mucosa regeneration.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AKT (also known as protein kinase B, PKB) plays an important role in cell survival or tumor progression. For these reasons, AKT is an emerging target for cancer therapeutics. Previously our studies showed that mitochondrial E3 ubiquitin protein ligase 1 (MUL1, also known as MULAN/GIDE/MAPL) is suppressed in head and neck cancer (HNC) and acts as negative regulator against AKT. However, the MUL1 regulatory mechanisms remain largely unknown. Here we report that cisplatin (CDDP) induces thyroid cancer cell death through MUL1-AKT axis. Specifically, CDDP-induced MUL1 leads to ubiquitylation of active form of AKT. We also observed that the role of forkhead box O3 (FOXO3) is pivotal in CDDP-induced MUL1 regulation. FOXO3 knock-downed cells show resistance against CDDP-mediated MUL1-AKT axis. CDDP-mediated intracellular ROS increment plays an important role in FOXO3-MUL1-AKT signal pathway. The data provide compelling evidence to support the idea that the regulation of FOXO3-MUL1-AKT axis can be a novel strategy for the treatment of HNC with CDDP.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.